drug Experts

Expert Opinion: DIY Peptide Injections Carry Risks Most People Never See Coming

Peptides are having a moment. People injecting them at home are chasing everything from weight loss and muscle recovery to sharper thinking and better sex drive. But according to UConn pharmacist and clinical pharmacologist C. Michael White, the bigger danger isn't just what's in the vial. It's what happens when untrained people try to draw up and inject these products themselves. White has been researching the gray markets for peptides, where companies sidestep FDA oversight by selling products labeled "for research purposes only." Because that labeling is a legal workaround, the companies can't legally tell buyers how to actually use what they're selling. "This means consumers must purchase any supplies they need and figure out the proper technique on their own," White writes. So he decided to test just how well people manage on their own. In a new study published in Public Health Reports, White and his colleagues recruited 20 people, 10 college students and 10 adults in their 60s, and asked each to reconstitute a semaglutide peptide product, draw it into a syringe, and inject a mannequin. They were allowed to research the process online or with AI beforehand. The results were rough. On average, both age groups got fewer than half the steps right. Some picked expired or cloudy dissolving liquid. Many miscalculated doses, couldn't clear air bubbles from the syringe, or injected into muscle instead of fat. Roughly half didn't know how to safely engage the needle's safety mechanism or dispose of it afterward. "These errors were serious and could increase the risk of infection, bleeding, over- or under-dosing, and needle sticks," White notes. What stood out most: Confidence didn't track with competence. After doing their homework, most participants in both groups felt "somewhat confident" they could do the injection correctly. Younger participants stayed confident even after fumbling through the process. Older adults, by contrast, adjusted their confidence downward once they saw how it actually went, which tracks with prior research showing older adults tend to be more accurate judges of their own ability on complex tasks. White's piece also digs into a potential fix on the table: In late July 2026, an FDA advisory panel recommended adding six widely used peptides, including BPC-157, TB-500, and Semax, to the list of substances compounding pharmacies can legally prepare. The panel's argument is that compounded versions would be safer than gray-market ones, since compounding pharmacies follow rules on sourcing and sterile production that the gray market doesn't. White isn't fully sold. Even if the FDA adopts the recommendation, he points out it would only apply to a handful of products, and it wouldn't change the fact that none of them have actually been tested for safety or effectiveness as finished drugs. The bulk of the gray-market risk stays exactly where it is. For more on the peptide boom and what the FDA is weighing, NBC News broke down the basics here: What are peptides and why is the FDA considering easing limits? Read the full article: Dr. White is Head and Distinguished Professor of the Department of Pharmacy Practice at the University of Connecticut, and co-director of the university's Health Outcomes, Policy, and Evidence Synthesis (HOPES) research group. His research focuses on drug, dietary supplement, and illicit drug safety, quality, and cost, with a specific throughline into adverse events tied to drugs, devices, herbal products, and substances of abuse. View complete profile He's a recurring voice on drug and supplement safety specifically, most recently quoted in Health magazine's "4 Major Risks of Unregulated Peptides" (Aug. 18, 2026) and on KCBS Los Angeles radio discussing GLP-1 drugs and youth mental health (Aug. 10, 2026). Dr. White is available for interviews on peptide safety, the gray-market supplement industry, GLP-1 and weight-loss drug trends, and drug/dietary supplement safety more broadly. Media can reach out by clicking this profile icon below.

National Cancer Research Month: Baylor Researchers at Forefront of New Discoveries

May is National Cancer Research Month, which highlights the importance of lifesaving research to the millions of people around the world affected by cancer. Thanks to spectacular advances made by cancer researchers, approximately 18.6 million people in the United States and millions more worldwide are living with, through and beyond their disease. Over the past year, Baylor University Media and Public Relations has reported on Baylor research at the forefront of discovering novel approaches to effective cancer therapies. University researchers are using tumor starvation techniques, natural products, phages, modified bacteria, precision nutrition and more in their trailblazing work on some of the most aggressive cancers, including kidney, pancreatic, oral, colorectal and breast cancers. In a recent article published by the University, it featured the hard work and research of eight Baylor experts driving those discoveries forward: • Kevin G. Pinney is developing a next-generation treatment for kidney cancer that targets the blood vessels feeding tumors. His research focuses on specialized drug conjugates designed to cut off oxygen and nutrients to renal cell carcinoma tumors — essentially starving cancer cells to death. • Daniel Romo is accelerating new therapies for pancreatic cancer using compounds derived from marine natural products. His work on a simplified version of pateamine A could offer a new therapeutic pathway for pancreatic ductal adenocarcinoma, one of the most aggressive and difficult-to-treat cancers. • Joseph Taube is investigating how breast cancers spread and resist treatment. His recent work examines whether a natural compound called Ophiobolin A can trigger inflammatory forms of cancer cell death that may work alongside immunotherapy — particularly in treatment-resistant triple-negative breast cancers. • Leigh Greathouse is combining cancer biology, nutrition science, and AI to personalize cancer prevention and treatment strategies. Her research explores how diet and the gut microbiome influence cancer outcomes and survivorship. • Michael S. VanNieuwenhze is leading groundbreaking colorectal cancer research using modified bacteria to deliver cancer-killing proteins directly into tumor cells. His team is engineering Listeria monocytogenes as a targeted therapeutic delivery system. • Aaron Wright is helping lead a major ARPA-H initiative exploring the use of bacteriophages — viruses that attack bacteria — to reshape the human microbiome and improve health. The project could eventually help prevent diseases linked to oral and colorectal cancers through low-cost phage-based treatments. • Savannah Rauschendorfer is researching how exercise interventions may reduce the harmful cardiac side effects of chemotherapy in adolescent and young adult cancer patients. Her work aims to identify patients at risk of cardiotoxicity earlier and improve long-term survivorship outcomes. • Jonathan Kelber studies the cellular and molecular mechanisms behind aggressive breast and pancreatic cancers. Through his Developmental Oncogene Laboratory, Kelber investigates how cancer cells evolve during tumor progression and tissue regeneration. Together, these researchers showcase how cancer science is rapidly evolving beyond traditional treatments – integrating biology, chemistry, nutrition, exercise science, microbiome research, and artificial intelligence in the search for more effective and personalized therapies.

Major trial shows increasing bone density fails to cut fracture risk in brittle bone disease

An international clinical trial involving Aston University researchers has challenged long held assumptions about how brittle bone disease is treated in adults, after finding that substantially increasing bone density did not reduce the risk of fractures. The study, published in the Journal of the American Medical Association (JAMA), examined whether a two stage treatment using the bone building drug teriparatide followed by the bone preserving drug zoledronic acid could reduce fractures in adults with osteogenesis imperfecta, often referred to as brittle bone disease, a rare genetic condition that causes bones to break easily throughout life. Researchers followed 349 adults treated at 27 specialist centres across the UK and Europe. While the treatment led to clear increases in bone density in the spine and hip, fracture rates were no lower than among patients receiving standard care, suggesting that bone quality may matter more than bone density alone in preventing fractures in people with the condition. The findings underline a key distinction between brittle bone disease and more common bone conditions such as osteoporosis, where increasing bone density is known to reduce fracture risk. In osteogenesis imperfecta, the study suggests that bones can become denser without becoming less likely to break, indicating that the underlying quality and structure of bone tissue may play a greater role in fracture risk than density alone. Dr Zaki Hassan Smith, an endocrinologist at Aston Medical School who contributed to the research, said: “This study shows that in osteogenesis imperfecta, simply increasing bone density doesn’t necessarily translate into fewer fractures. That’s important, because it tells us that the disease is more complex than what we see on a scan. The findings help shift the focus towards understanding bone quality and how bones behave in real life, which is essential if we are to develop more effective treatments that genuinely reduce harm for patients.” Osteogenesis imperfecta is a genetic condition that affects collagen, leaving bones fragile and prone to fracture throughout life. There is currently no licensed treatment specifically approved to prevent fractures in adults with the condition, and patients often experience repeated fractures, chronic pain and long term disability. The trial tested a sequential treatment strategy commonly used in osteoporosis, where a bone building drug is followed by a treatment designed to preserve gains in bone strength. Although this approach successfully increased bone density in people with osteogenesis imperfecta, it did not reduce fracture rates, suggesting that treatment strategies effective in osteoporosis may not directly translate to rare bone diseases. Researchers did observe improvements in some quality of life measures among participants receiving the treatment, including reduced pain interference and improved mobility. However, fracture prevention remained unchanged, reinforcing the need for new approaches that target the fundamental properties of bone in osteogenesis imperfecta rather than density alone. The study was led by the University of Edinburgh and funded by the Medical Research Council and the National Institute for Health and Care Research. Aston University contributed clinical and academic expertise through Aston Medical School as part of the large international collaboration, which involved specialist centres across the UK and Europe. The study was led by the University of Edinburgh, with Aston University contributing clinical and academic expertise as part of a wider international collaboration involving multiple specialist centres across the UK and Europe. The research was funded by the Medical Research Council and the National Institute for Health and Care Research. Researchers say the findings provide important guidance for future research, helping to steer efforts towards treatments that focus on bone quality, strength and resilience in everyday life. They also highlight the value of large scale clinical trials in rare diseases, where learning what does not reduce harm is an essential step towards better care. The paper, Teriparatide Plus Zoledronic Acid for Osteogenesis Imperfecta, is published in JAMA. https://doi.org/10.1001/jama.2026.6889

CEOs 5 times more likely to survive fraud than a personal scandal

If the CEO of Astronomer had overseen tax fraud instead of being caught on a kiss cam cuddling his HR chief in an extramarital affair, he might still have a job. That’s because, according to a new study, CEOs are five times more likely to be fired for personal misconduct than for overseeing financial fraud. “For financial fraud, the CEO can easily say, ‘Hey, it wasn’t me,’” said Aaron Hill, Ph.D., an associate professor in the University of Florida Warrington College of Business who led the study. “With personal misconduct, there’s no excuse.” The research, forthcoming in Strategic Organization, examined 59 cases of personal misconduct and compared them with more than 300 financial scandals at publicly traded companies between 1997 and 2020. The personal cases included inappropriate relationships, drug or alcohol incidents, domestic violence, falsifying credentials and derogatory speech. Hill and his colleagues found that boards move decisively when a CEO’s private behavior becomes public. By contrast, financial misconduct — such as accounting restatements that can wipe out billions in shareholder value — often leaves room for a chief executive to deflect blame onto others in the organization. Recent company performance influenced how boards responded, to a point. A CEO whose company was thriving could often survive a financial scandal because directors had both plausible deniability and a strong incentive not to disrupt success. But good numbers offered little protection when the problem was personal behavior. For example, McDonald’s ousted Steve Easterbrook in 2019 over a consensual relationship with a subordinate, even though the company’s stock price had doubled under his leadership. Hewlett-Packard similarly dismissed CEO Mark Hurd after harassment allegations despite his reputation for turning the firm around. “Even strong performance can’t erase certain kinds of misconduct,” Hill said. “There are some things you just can’t excuse.” The study also uncovered how scandals influenced succession decisions. When personal misconduct led to a firing, boards were more likely to promote an insider, signaling that the problem lay with one person rather than the culture of the company. Financial scandals, on the other hand, often prompted boards to recruit outsiders as a way of reassuring markets that the firm was serious about change. “It’s a signaling move,” Hill said. “Bring in an outsider after fraud, and the market reacts positively. Stick with an insider after a personal scandal, and it says the organization itself is sound.” The researchers argue that these choices reveal how boards balance their fiduciary duty with the reputational risks of scandal. While dismissing a CEO can serve as a public relations reset, Hill emphasized that it is almost always a financially motivated calculation. “Boards are supposed to look out for the company and its shareholders,” he said. “But when they decide to keep a CEO after misconduct, I think it sends the wrong message — to employees, to investors and to the public.”

Discovery pinpoints potential Achilles’ Heel in HIV, opening new frontier in drug development

Scientists have long known that detecting HIV early is crucial in slowing and treating the virus. During the acute stage of infection, a single human cell can produce as many as 10,000 new HIV particles. A discovery led by the University of Delaware's Juan Perilla offers hope: A new drug target early in the virus's life cycle that could save millions of lives. In the surprising discovery, published Feb. 18 in Nature, Perilla and collaborators in the U.S. and the United Kingdom, have revealed a previously unknown role for the viral protein integrase. Scientists already knew that integrase helps HIV insert itself into human DNA. But this new study provides the first direct evidence that integrase plays a critical structural role earlier on in HIV’s life cycle — when the virus matures into an infectious force. Using high-resolution cryo-electron microscopy (cryo-EM), the research team – which also included UD doctoral student Juan S. Rey – found that integrase proteins form gluey filaments that line the inside of the capsid. Each segment of the filament slots neatly into the capsid’s hexagon-shaped tiles, while gripping tightly to HIV’s RNA genome. This zipper-like arrangement organizes and packs the virus, preparing it to hijack a cell and start making copies of itself. “Integrase plays a structural role inside the HIV capsid — nobody expected that,” Perilla said. “This protein forms filaments that anchor the RNA to the capsid. Without these filaments, the virus is non-infective.” Seeing inside HIV is no small feat. The capsid is only about 120 nanometers wide —roughly 1/800th the thickness of a human hair. It is incredibly small, fragile, densely packed and constantly changing, Perilla said. To reveal its hidden architecture, the researchers relied on deep collaboration and a combination of sophisticated microscopy, molecular modeling and experimentation. Read more about the science behind the study here. “The thing with HIV is that people are chronically living with it,” Perilla said. “Treatments are effective, but patients always need new therapeutics. We want to help develop the next generation of inhibitors and hope to have a significant contribution.” To reach Perilla directly and arrange an interview, visit his profile page. Interested reporters can also email MediaRelations@udel.edu.

Surprising finding could pave way for universal cancer vaccine

An experimental mRNA vaccine boosted the tumor-fighting effects of immunotherapy in a mouse-model study, bringing researchers one step closer to their goal of developing a universal vaccine to “wake up” the immune system against cancer. Published today in Nature Biomedical Engineering, the University of Florida study showed that like a one-two punch, pairing the test vaccine with common anticancer drugs called immune checkpoint inhibitors triggered a strong antitumor response in laboratory mice. A surprising element, researchers said, was that they achieved the promising results not by attacking a specific target protein expressed in the tumor, but by simply revving up the immune system — spurring it to respond as if fighting a virus. They did this by stimulating the expression of a protein called PD-L1 inside of tumors, making them more receptive to treatment. The research was supported by multiple federal agencies and foundations, including the National Institutes of Health. Senior author Elias Sayour, M.D., Ph.D., a UF Health pediatric oncologist and the Stop Children's Cancer/Bonnie R. Freeman Professor for Pediatric Oncology Research, said the results reveal a potential future treatment path — an alternative to surgery, radiation and chemotherapy — with broad implications for battling many types of treatment-resistant tumors. “This paper describes a very unexpected and exciting observation: that even a vaccine not specific to any particular tumor or virus — so long as it is an mRNA vaccine — could lead to tumor-specific effects,” said Sayour, principal investigator at the RNA Engineering Laboratory within UF’s Preston A. Wells Jr. Center for Brain Tumor Therapy. “This finding is a proof of concept that these vaccines potentially could be commercialized as universal cancer vaccines to sensitize the immune system against a patient’s individual tumor,” said Sayour, a McKnight Brain Institute investigator and co-leader of a program in immuno-oncology and microbiome research. Until now, there have been two main ideas in cancer-vaccine development: To find a specific target expressed in many people with cancer, or to tailor a vaccine that is specific to targets expressed within a patient's own cancer. “This study suggests a third emerging paradigm,” said Duane Mitchell, M.D., Ph.D., a co-author of the paper. “What we found is by using a vaccine designed not to target cancer specifically but rather to stimulate a strong immunologic response, we could elicit a very strong anticancer reaction. And so this has significant potential to be broadly used across cancer patients — even possibly leading us to an off-the-shelf cancer vaccine.” For more than eight years, Sayour has pioneered high-tech anticancer vaccines by combining lipid nanoparticles and mRNA. Short for messenger RNA, mRNA is found inside every cell — including tumor cells — and serves as a blueprint for protein production. This new study builds upon a breakthrough last year by Sayour’s lab: In a first-ever human clinical trial, an mRNA vaccine quickly reprogrammed the immune system to attack glioblastoma, an aggressive brain tumor with a dismal prognosis. Among the most impressive findings in the four-patient trial was how quickly the new method — which used a “specific” or personalized vaccine made using a patient’s own tumor cells — spurred a vigorous immune-system response to reject the tumor. In the latest study, Sayour’s research team adapted their technology to test a “generalized” mRNA vaccine — meaning it was not aimed at a specific virus or mutated cells of cancer but engineered simply to prompt a strong immune system response. The mRNA formulation was made similarly to the COVID-19 vaccines, rooted in similar technology, but wasn’t aimed directly at the well-known spike protein of COVID. In mouse models of melanoma, the team saw promising results in normally treatment-resistant tumors when combining the mRNA formulation with a common immunotherapy drug called a PD-1 inhibitor, a type of monoclonal antibody that attempts to “educate” the immune system that a tumor is foreign, said Sayour, a professor in UF’s Lillian S. Wells Department of Neurosurgery and the Department of Pediatrics in the UF College of Medicine. Taking the research a step further, in mouse models of skin, bone and brain cancers, the investigators found beneficial effects when testing a different mRNA formulation as a solo treatment. In some models, the tumors were eliminated entirely. Sayour and colleagues observed that using an mRNA vaccine to activate immune responses seemingly unrelated to cancer could prompt T cells that weren’t working before to actually multiply and kill the cancer if the response spurred by the vaccine is strong enough. Taken together, the study’s implications are striking, said Mitchell, who directs the UF Clinical and Translational Science Institute and co-directs UF’s Preston A. Wells Jr. Center for Brain Tumor Therapy. “It could potentially be a universal way of waking up a patient’s own immune response to cancer,” Mitchell said. “And that would be profound if generalizable to human studies.” The results, he said, show potential for a universal cancer vaccine that could activate the immune system and prime it to work in tandem with checkpoint inhibitor drugs to seize upon cancer — or in some cases, even work on its own to kill cancer. Now, the research team is working to improve current formulations and move to human clinical trials as rapidly as possible. While the experimental mRNA vaccine at this point is in early preclinical testing — in mice not humans — information about available nonrelated human clinical trials at UF Health can be viewed here.

Experts in the Media: What You Need to Know About Medication Safety and Everyday Health

From medication safety to seasonal illness prevention, pharmacists are often the most accessible, and overlooked,  healthcare professionals in our communities. In a recent segment on NBC, Dr. Shannon Yarosz breaks down common misconceptions about prescriptions, explains how drug interactions really work, and shares practical advice patients can use immediately to better manage their health. Dr. Shannon Yarosz is an Assistant Professor of Pharmacy Practice. Prior to joining the faculty at Cedarville University, served in multiple pharmacy roles. Her career reflects a deep commitment to patient care with experience in pediatrics, community pharmacy practice, and clinical healthcare services. As healthcare systems face growing pressure and patients navigate increasingly complex medication regimens, pharmacists are playing a larger role than ever before. This discussion highlights why their expertise matters, from helping patients avoid costly mistakes to providing front-line guidance on everyday health concerns. When should I stop taking antibiotics? Is it ok to stop when I begin feeling better? This question and several others were addressed in this week's Ask the Pharmacist segment on WDTN TV in Dayton, Ohio. Looking to know more or connect with Dr. Shannon Yarosz? Simply contact: Mark D. Weinstein Executive Director of Public Relations Cedarville University mweinstein@cedarville.edu

Study: What makes a smell bad?

You wouldn’t microwave fish around your worst enemy — the smell lingers both in kitchen and memory. It is one few of us like, let alone have positive associations with. But what makes our brains decide a smell is stinky? A new study from UF Health researchers reveals the mechanisms behind how your brain decides you dislike — even loathe — a smell. Or as first author and graduate research fellow Sarah Sniffen puts it: How do odors come to acquire some sort of emotional charge? In many ways, our world capitalizes upon the importance of smells to influence emotions, running the gamut from perfumes to cooking and even grocery store design. “Odors are powerful at driving emotions, and it’s long been thought that the sense of smell is just as powerful, if not more powerful, at driving an emotional response as a picture, a song or any other sensory stimulus,” said senior author Dan Wesson, Ph.D., a professor of pharmacology and therapeutics in the UF College of Medicine and interim director of the Florida Chemical Senses Institute. But until now, researchers have puzzled over what circuitry connects the parts of the brain vital to generating an emotional response with those responsible for smell perception. The team started off with the amygdala, a brain region that curates your emotional responses to sensory stimuli. Although all our senses (sound, sight, taste, touch and smell) interact with this small part of your brain, the olfactory system takes a more direct route to it. “This is, in part, what we mean when we say your sense of smell is your most emotional sense,” Sniffen said. “Yes, smells evoke strong, emotional memories, but the brain’s smell centers are more closely connected with emotional centers like the amygdala.” In the study, researchers looked at mice, who share neurochemical similarities with people. They can learn about odors and categorize them as good or bad. After observing their behavior and analyzing brain activity, the team found two genetically unique brain cell types that allow odors to be assigned into a bucket of good feelings or bad feelings. Initially, the team expected that one cell type would generate a positive emotion to an odor, and another would generate a negative emotion. Instead, the brain’s cellular organization gives the cells the capability of doing either. “It can make an odor positive or negative to you,” Wesson said. “And it all depends upon where that cell type projects in your brain and how it engages with structures in your brain.” But why is knowing more about how we categorize smells important? Well, for starters, smells — and our reactions to them — are a part of life. Sometimes, however, our reactions to them can be outsized, or take on a negative association so strong it disrupts how we live. “We’re constantly breathing in and out and that means that we’re constantly receiving olfactory input,” Sniffen said. “For some people that’s fine, and it doesn’t impact their day-to-day life. They might even think, ‘Oh, odors don’t matter that much.’ But for people who have a heightened response to sensory stimuli, like those with PTSD or anxiety or autism, it’s a really important factor for their day-to-day life.” In the future, the research could help clinicians adjust for heightened sensory response that some people struggle with in their everyday lives, Wesson added. One example? A patient associating a clinic’s smell with transfusions that made them queasy. Based upon the receptor systems in these specific brain pathways, the team members believe they might be able to change those associations. Potentially, medications could suppress some of these pathways’ activity to allow you to overcome stressful and aversive emotional responses. Conversely, these pathways could be activated to restore enjoyment to things that people might have grown indifferent to — like those who lose their appetite from illness. “Emotions in part dictate our quality of life, and we’re learning more about how they arise in our brain,” Wesson said. “Understanding more about how our surroundings can impact our feelings can help us become happier, healthier humans.” This research was supported by funding from the National Institute on Deafness and Other Communication Disorders and the National Institute on Drug Abuse. Sarah Sniffen was supported by a fellowship from the National Institute on Deafness and Other Communication Disorders.

Gene Editing Breakthrough Offers New Hope for Head and Neck Cancer Patients

Researchers at the ChristianaCare Gene Editing Institute have made an important advance in treating head and neck cancers. By using CRISPR gene editing, the team found a way to restore how well chemotherapy works in tumors that have stopped responding to treatment. Their results, now published in Molecular Therapy Oncology, could change how doctors treat these aggressive cancers and give new hope to many patients who face limited options. Head and neck cancer is the seventh most common cancer worldwide, and cases are expected to rise by 30 percent every year by 2030. Even with progress in surgery, chemotherapy and immunotherapy, many patients still reach a point where treatment no longer works. The ChristianaCare team aimed to solve this challenge at its source. Targeting the Heart of Drug Resistance The researchers focused on a gene called NRF2. This gene acts like a master switch that helps cancer cells survive stress and resist chemotherapy. Because NRF2 plays such a central role in tumor growth, the team chose to develop a genetic therapy that disables the gene itself rather than targeting a single protein, which is common in traditional drug development. Since NRF2 is a transcription factor, shutting it down in a lasting way is more likely to succeed through CRISPR gene editing. Their major advance was showing that CRISPR can successfully disrupt NRF2 in head and neck cancer cells and in esophageal cancer cells. This work builds on earlier studies in lung cancer, where blocking NRF2 made tumors more sensitive to chemotherapy and improved survival in animal models. “Our goal was to break through the wall of drug resistance that so many patients face,” said Natalia Rivera Torres, Ph.D., the study’s lead author. “By precisely editing the NRF2 gene, we can make cancer cells vulnerable again to standard treatments. This could improve outcomes and quality of life.” Precision Matters: The Power of Target Choice The study also showed that the location of the CRISPR cut within the NRF2 gene makes a big difference. The strongest results came from targeting exon 4, a part of the gene that controls a key section of the NRF2 protein. Editing this region reduced NRF2 levels by 90 percent and made cancer cells much more sensitive to chemotherapy. In comparison, editing exon 2 was less effective even though it still caused high levels of gene disruption. The team also found that a process called exon skipping, where sections of genetic code are rearranged, can affect the outcome of gene editing. This discovery highlights how important careful design and testing are when building gene editing therapies. A Platform for Broader Impact ChristianaCare researchers saw the same results in both head and neck cancer cells and esophageal cancer cells. This suggests the strategy could help treat many solid tumors that have high levels of NRF2 and are known for strong drug resistance. “This is more than just a single experiment,” said Eric Kmiec, Ph.D., director of the Gene Editing Institute and senior author of the study. “We are building a platform that can be adapted to different cancers. Our earlier work in lung cancer showed the promise of this approach, and now we see it working in other hard to treat tumors. It is an exciting step toward making gene editing a meaningful part of cancer treatment.” Looking Ahead: Toward Clinical Application With these strong results, the team is now focused on finding the safest and most effective way to deliver the gene editing tools directly to tumors. Their goal is to reduce how much standard treatment a patient needs in order to get the best result with fewer side effects. “Drug resistance is one of the biggest challenges in cancer care,” Rivera Torres said. “If we can overcome it with gene editing, we could give patients more time, better quality of life and a renewed sense of hope.” Kmiec added, “We are committed to moving this technology forward quickly while always keeping the patient in mind. The future of cancer treatment is personal, precise and, we believe, within reach.”

Maduro is gone; expert details potential impact on the Caribbean

Globally, the ousting of Nicolás Maduro in Venezuela has been met with a mix of reactions and cautious optimism. The University of Delaware’s Kalim Shah can discuss how regime change will play across the Caribbean and the spillover effect that will ripple throughout the region – and the world – in the years and decades to come. Shah, professor of energy and environmental policy and an expert on the island nations of the Caribbean, says that although public statements have been muted and restrained, there is a shared understanding. “For small island states that have absorbed the effects of Venezuelan collapse for more than two decades, this moment represents the possible end of a long and destabilizing chapter,” Shah said. Caribbean governments are not celebrating regime change, Shah said. Rather, they are responding to the prospect of reduced systemic risk. “A Venezuela that no longer exports large-scale displacement, opaque energy leverage and permissive criminal governance is objectively preferable for the region.” Shah can discuss several aspects of Venezuela’s political history, how the nation has arrived where it is, where it might be headed and the impact this will have on the Caribbean as a whole. Those include: • Venezuela’s political and economic deterioration during the Chávez–Maduro era and how that has translated directly into pressures felt across the Caribbean in the form of migration, fiscal exposure, security risks and regional uncertainty. • How the nation’s institutional collapse coincided with deepening organized crime activity across the Caribbean basin. Data from the United Nations Office on Drugs and Crime consistently places the region within major cocaine trafficking corridors linking South America with North American and European markets. For Caribbean governments, this meant higher interdiction costs, increased exposure to transnational criminal networks and growing pressure on already limited security institutions. • This moment invites a reassessment of China’s expanding footprint in the Caribbean, Shah says. He can discuss the ways in which Beijing has deepened its presence throughout the region. Shah says that as this transition unfolds, five policy developments will determine whether the cautious optimism proves warranted: • The impact on Venezuelan outward migration to the Caribbean. • Whether Caribbean public systems receive durable support rather than short-term humanitarian fixes. • Organized crime and drug trafficking pressures in the Caribbean basin. • External security engagement in the Caribbean. • Whether the region avoids a return to dependency-driven energy and infrastructure politics. “For the Caribbean, hope today is not naïve. It is conditional. The Chávez–Maduro years imposed real costs on the region. Their end creates an opening…but only if policy follows through,” Shah said. To contact Shah directly for interviews, visit his expert page and click on the "contact" button. Interested reporters can also send an email to mediarelations@udel.edu.